and growth factors, epithelial and interstitial cell changes would ultimately lead to the tubulointerstitial lesions that are part of the end-stage kidney.
was supported by USPHS NIDDK grants: #DK37097, and I wish to thank Ms Judy Hurst for her assistance in the preparation of this manuscript and my collaborators in the Vanderbilt Kidney and Urologic Disease Center for their support.
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Chronic renal failure: management
An increased serum urea or creatinine concentration indicates impaired renal function. Identification of the cause of the renal insufficiency, as well as secondary factors contributing to it, will help classify the condition as acute or chronic. Although acute and chronic renal disease states do not have mutually exclusive causes, the diagnosis of chronic renal disease can be established, firstly, by assessment of the extent and severity of the disease-eg, diabetes or glomerulonephritis-that underlies renal damage and, secondly, by showing the constant presence and progressive nature of the renal impairment. In kidney diseases characterised by irreversible injury, once a critical amount of functional renal loss has taken place, progression to end-stage disease seems common, even if the initiating event or condition is resolved or eradicated. Moreover, of the cause of chronic renal failure, several irrespective intercurrent events (table i) may accelerate the rate of loss of renal function. These events may lead to either a transient or a permanent loss of renal function. The importance of such intercurrent events cannot be overemphasised because their detection and correction may slow the progression of renal insufficiency and delay the need for renal replacement
progression of chronic renal failure is best assessed by sequential measurements of glomerular filtration rate (GFR) with exogenous markers such as inulin, 1251iothalamate, 9